Diabetes, Vol 30, Issue 4 310-313, Copyright © 1981 by American Diabetes Association
The mechanism of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis
MS Oh, MA Banerji and HJ Carroll
To determine the mechanism of hyperchloremic acidosis during recovery from
diabetic ketoacidosis (DKA), serial measurements were made in eight
patients of serum and urinary electrolytes and organic acids, and of
urinary net acid. On admission, the average decrease in serum total CO2 was
17.5 mmol/L, corresponding to the excess anion gap, 18.5 meq/L, and the
serum organic acids, 17.1 meq/L. With the treatment, the anion gap and
organic acids decreased by 16.1 and 14.7 meq/L, respectively, but the serum
CO2 increased only by 8.4 mmol/L; serum electrolyte balance was maintained
by increase in chloride concentration. Fluid retention was insufficient to
explain the disparity between the increase in CO2 and the decrease in
organic acids. Renal loss of bicarbonate precursors during treatment was
modest and was exceeded by renal bicarbonate production. The disparity
between the increase in serum CO2 and the decrease in organic acids during
treatment of DKA may be explained to a large extent by a difference in
volume of distribution between bicarbonate and organic anions. The renal
loss of ketone anions before admission, however, is ultimately responsible
for the persistence of substantial metabolic acidosis.